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High activity of fatty acid oxidation enzymes in human placenta: Implications for fetal‐maternal disease
Author(s) -
Oey N. A.,
Den Boer M. E. J.,
Ruiter J. P. N.,
Wanders R. J. A.,
Duran M.,
Waterham H. R.,
Boer K.,
der Post J. A. M.,
Wijburg F. A.
Publication year - 2003
Publication title -
journal of inherited metabolic disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 102
eISSN - 1573-2665
pISSN - 0141-8955
DOI - 10.1023/a:1025163204165
Subject(s) - placenta , fetus , metabolic disease , enzyme , beta oxidation , human genetics , disease , pregnancy , human placenta , medicine , biochemistry , biology , endocrinology , genetics , gene
Abstract As the human fetus and placenta are considered to be primarily dependent on glucose oxidation for energy metabolism, the cause of the remarkable association between severe maternal pregnancy complications and the carriage of a fetus with an inborn error of mitochondrial long‐chain fatty acid oxidation (FAO) has remained obscure. We analysed human term placenta and chorionic villus samples for the activities of a variety of enzymes involved in FAO, and compared the results with those obtained in human liver. All enzymes were found to be expressed, with a very high activity of two enzymes involved in the metabolism of long‐chain fatty acids (CPT2 and VLCAD), whereas the activity of medium‐chain acyl‐CoA dehydrogenase (MCAD) was found to be low, when compared to liver. These results suggest that fatty acid oxidation may play an important role in energy generation in human placenta, and that a deficiency in the placental oxidation of long‐chain FAO may result in placental dysfunction, thus causing gestational complications.